Tag: openaccess

June 12, 2014 ScienceEveryday (medical imaging is separate) Post a Comment

Breaking the hype before it spreads too fast

Breaking the hype before it spreads too fast

Well done, Buddhini Samarasinghe.

#ScienceEveryday  

Originally shared by Buddhini Samarasinghe

Pulling a Fast One on Cancer

There is a report making the rounds on social media that really needs to be explained, because as usual the media hype is distorting the findings. The article in question was published in the Cell Stem Cell journal, and is #OpenAccess (http://goo.gl/pnoiwa). I will explain the background, what these results mean, and more importantly, what they don’t mean.

✤ Traditional chemotherapy is toxic to cells. The only reason traditional chemotherapy works is because it kills cancer cells faster than it kills normal cells. The side effects from chemo often happen because normal cells are also affected. One such side effect is the suppression of the immune system. This happens because chemo damages adult stem cells too, which impairs tissue repair and regeneration. 

✤ Blood stem cells (known as hematopoietic stem cells) are responsible for replacing our blood cells; these reside in the bone marrow. In this study, scientists investigated the effect of prolonged fasting on hematopoietic stem cells.

✤ Mice used in this study were fasted for 48 hours, which the scientists defined as prolonged fasting. These mice received no food, only water. They then treated the mice with cyclophosphamide, a common chemotherapy drug. They found that cycles of prolonged fasting reduced the damage caused to hematopoietic stem cells when the mice were treated with cyclophosphamide. They also found that prolonged fasting cycles promoted the regeneration of blood cells through the protection of hematopoietic stem cells. 

✤ Next, the scientists tested whether the effects of prolonged fasting were independent of the toxic side effects of chemotherapy. Could prolonged fasting alone stimulate hematopoietic stem cells to self-renew? Indeed, it could. 

✤ What is the molecular mechanism for this process? A growth factor known as Insulin-like Growth Factor-1 (IGF-1) seemed to be involved. Growth factors are proteins that control the multiplication of cells. To examine this mechanism, the scientists used mice that were deficient in IGF-1.  If you’re curious about how these ‘knockout mice’ are generated, read http://goo.gl/jdbqbk. When these IGF-1 deficient mice were treated with cyclophosphamide, they showed similar results to the prolonged fasting mice; reduced levels of hematopoietic stem cell damage. So getting rid of IGF-1 induced the same protective effects on hematopoietic stem cells.  

✤ How does IGF-1 signalling protect hematopoietic stem cells? They found that the activity of an enzyme known as PKA was also reduced in these prolonged fasting/IGF-1 deficient mice. PKA controls the pathway involved in stem cell regeneration. So inhibiting IGF-1 or PKA signalling mimics the effect of prolonged fasting; it promotes the regeneration of hematopoietic stem cells, thereby reducing the immuno-suppressive side effect of chemotherapy. 

✤ This is really interesting data – this research has identified one of the signalling pathways in the intricate network of reactions controlling the behaviour of hematopoietic stem cells. The mechanism involves PKA and IGF-1 signalling.  

WHAT THE DATA DOESN’T SHOW

What this doesn’t show is that fasting is magically a cure-all for cancer. There isn’t a single study that shows lowered incidence of cancer in human populations that fast regularly. The fasting that these mice underwent also did not include the feasting that goes on every night as seen with human populations either. The scientists also conducted a small Phase I clinical trial in which patients undergoing chemotherapy fasted for 72h – the results are promising; their hematopoietic stem cells were protected when compared with the non-fasting control group. But obviously more data is needed, and it is highly inadvisable to fast before undergoing chemo, without the explicit guidance of a physician.

To summarise, fasting is not a cure for cancer. If anything, fasting does “cure” everything, eventually; this pathway involves a mechanism known as ‘death’. 

Image: fasting causes a major reduction in white blood cells followed by their replenishment after refeeding. These effects of prolonged fasting can result in the reversal of chemotherapy-induced immunosuppression. 

Image source: http://goo.gl/pnoiwa

#ScienceMediaHype   #ScienceEveryday  

December 8, 2013 ScienceEveryday (medical imaging is separate) Post a Comment

Let me echo what Samantha Andrews posted

Let me echo what Samantha Andrews posted

This is a fantastic post about underwater noise pollution. It’s been going on for years and still does not receive enough attention. I had been planning on my own post with the links below but Samantha Andrews did such a tremendous job, I’ll simply echo her post.

Here are some additional links.

Noise Pollution Could Frustrate Fish

http://goo.gl/ix66EO via WIRED 

With Noise Pollution Growing at Sea, A Texas Team Looks for Answers

http://goo.gl/M6QNmW via State Impact an NPR reporting arm

Science Update – Aquatic Noise Pollution

http://goo.gl/7jFpqm via Naked Scientists

#ScienceSunday 

Originally shared by Samantha Andrews

Most of us have been there.  You’re in a pub or a club trying to have a conversation but the music…it’s just too loud to hear what the other person is saying.  You shout louder and louder, the listener has their ear up close to your mouth but alas, the conversation doesn’t flow as it would do if you could both hear each other easily.  Now imagine that sound wasn’t just important for having a conversation, but for seeing.  And imagine that that loud noise preventing you from hearing properly wasn’t just in the pub, but occurred throughout your day-to-day activities.  

Noise pollution is a problem for cetaceans because they use echolocation to ‘see’ and hear.  It’s quite a nifty technique because often the ocean is too murky or too dark for your eyes to see very far in, but sound can still travel.  Thanks to evolution, cetaceans have echolocation down to a fine art.  Not only can they figure out that something is there, but they can work out what it is.  But when it’s too noisy, the echolocation process can be disrupted and activities like hunting, navigation, and pod communication can become difficult to impossible.  Noise has even been linked to stress, and increased energy expenditure in our aquatic brethren.  One of the problems with figuring out just how noise pollution is affecting cetaceans is a lack of baseline data – to a large extent we don’t know the status of cetacean populations inhabiting different areas.  When we do get around to taking measurements of noise, we don’t have a good handle on how noisy different areas were in the first place to know if the noise has increased.  This lack of baseline data includes in conservation areas designated as important marine mammal habitat – just like the Moray Firth up in Scotland.  

The Moray Firth is home to a well-studied population of bottlenose dolphins (Tursiops truncates), but it also has strategic importance, forming a base for North Sea oil and gas exploration and potentially in the future, a base for an offshore wind farm.  Noise is likely to increase but to figure out by just how much Nathan Merchant of the University of Bath, alongside Enrico Pirotta, Tim Baron, and Paul Thompson of the University of Aberdeen decided to get some baseline data before developments begin.  Once that data is in place, they argue, more accurate correlations between noise and effects of marine mammals can be determined.

During the summer of 2012, Nathan and his team placed two underwater noise monitors – both in deep narrow channels popular with the dolphins for foraging, as well as prime shipping traffic routes.  They then monitored the noise on a cycle of 1 minute every 10 minutes and tied that data up with Automatic Identification System (AIS) ship-tracking data.  For the other 9 minutes recordings still took place, primarily to provide more analysis of noise events of interest.  And of course, this sound recordings also picked up the bottlenose dolphins as well as other marine mammals, but the team also deployed C-Pods – recorders dedicated for marine mammal noise – at the sites.  Conditions like rain and wind can also create noise in the Firth so meteorological data was also collected.

The acoustic data confirmed that the dolphins were using the two site quite heavily, with recordings of their clicks at both sites being made every day.  The two sites differed a fair bit in their baseline noise levels, with one generally much noisy than the other, with shipping traffic appeared to be the main source of noise pollution.  The researchers hypothesise that increase in noise levels at the already noisy site may be less damaging to the dolphins than increases at the quieter site, because the noisy site has already suffered noise-related habitat degradation to which the dolphins have already become accustomed.  Indeed the Moray Firth population size is showing signs of being stable, and is perhaps even increasing which is a positive sign.  However, the dolphin vocalizations overlapped both in frequency and amplitude with the shipping traffic.  This is concerning because it means that there is a higher risk of the dolphin’s vocalization being masked out by increases in shipping traffic.  Just how much shipping noise is too much is still unclear.

The paper is published in the journal Marine Pollution Bulletin and has been made open access.  You can read it here: http://dx.doi.org/10.1016/j.marpolbul.2013.10.058

There are also a couple videos up on youtube where you can listen to “short real-time clips” of the ship noise monitoring in the Moray Firth, accompanied by ship tracking data, underwater recorders, and time-lapse cameras.  Check them out here Ship noise monitoring in the Moray Firth – The Sutors and here Ship noise monitoring in the Moray Firth – Chanonry

Image: Campaign image from the Whale and Dolphin Conservation Society (www.wdcs.org)

#marinescience   #sciencesunday   #dolphins   #noisepollution #openaccess  

April 3, 2013 ScienceEveryday (medical imaging is separate) Post a Comment

You can’t silence science around Wonder Woman

You can’t silence science around Wonder Woman

Happy birthday Rajini Rao have a #punderstorm  day, especially #ScienceEveryday with the #Incorrigibles.

#Wolverine2WonderWomanHappyBD

Originally shared by Buddhini Samarasinghe

Interfering with RNA

A birthday tribute to someone I really admire here on G+, who is an amazing mentor and friend. Happy Birthday Rajini Rao, hope you have a wonderful year ahead and it’s been a pleasure knowing and working with you on our many projects together on G+!

A few days ago during our ENCODE Hangout on Air (http://goo.gl/H6KDE), I mentioned microRNAs. I wanted to write a post today about the general mechanism of how a gene can be ‘silenced’ through a process known as RNA interference.

• As we explained during the Hangout, the Central Dogma of Molecular Biology is DNA –> RNA –> Protein. This means the DNA blueprint makes a sequence-specific copy of RNA, which in turn acts as a blueprint for a specific sequence of amino acids which make up a protein. 

• So imagine if you could somehow destroy the RNA blueprint (known as the messenger RNA, or mRNA) for a particular protein. This would prevent the protein from being made – no blueprint, no protein. This is what RNA interference, or gene silencing is.

• It was first observed by plant scientists working on petunias in 1990. They were trying to make the color of the flower darker, so they introduced extra copies of the gene chalcone synthase, a key enzyme involved in the synthesis of pink and violet flower pigment (http://goo.gl/2A0Wk). Their logic makes sense – adding more copies of the gene for chalcone synthase should make more protein, which in turn should make flowers darker. But when they did the experiment, instead of darker flowers they got lighter flowers, or fully or partially white flowers absent of any color (see image below). Clearly, introducing extra copies of the chalcone synthase gene was decreasing the activity of chalcone synthase. 

• Similar phenomena were reported in fungi, and also in plant viruses. However, it was not until 1998 when Andrew Fire and Craig Mello formally identified the process as ‘RNA interference’ in their groundbreaking work on the nematode worm  Caenorhabditis elegans (http://goo.gl/XYId1). They injected sequence specific double-stranded DNA into the worm and then observed the silencing of the target gene (the mRNA blueprint went missing, and therefore so did the protein). This was the first time that double-stranded DNA was identified as the causative agent for the gene silencing phenomenon.

• The discovery completely revolutionized biology; Fire and Mello were awarded the Nobel Prize just eight short years after the publication of their work, which is very unusual (usually Nobel-prizes recognize work that is several decades old!). The work was so important because now we could silence any gene to see the effect it would have on the organism.

• Why is this important? Imagine you have a car, and you want to learn the function of the different parts. If you remove (or silence!) a wheel, the car cannot move. Therefore you can conclude that the wheel is necessary for motion. The same could be done within the organism; silence a gene, and you notice that the animal is now impaired in movement, so you can conclude that the gene may be involved in muscle development or coordination. Silence another gene, and you notice the eggs look strange, and you conclude that the gene was involved in egg development. RNA interference allowed scientists to assign a function to a gene; this has been and will remain an invaluable tool in molecular biology for decades ahead.

All the original research papers I’ve cited above are #openaccess  

Image credit: http://goo.gl/Ry6U3

#ScienceEveryday    #Wolverine2WonderWomanHappyBD